Using extracellular single unit recording techniques we have found that cholcystokinin (CCK) modulates the sensitivity of dopamine (DA) autoreceptors in the substantia nigra. Systemically administered CCK produces a DA autoreceptor supersensitivity. This supersensitivity may explain CCK's putative antipsychotic effect. We have also found that CCK excites neurons in the olfactory tubercule, and that only those neurons which are inhibited by the DA agonist apomorphine are excited by CCK. In addition to studying CCK/DA interaction, we have also been attempting to determine whether systemically administered CCK acts directly in the brain or through some peripheral mechanism. We have found that neither acute nor chronic vagotomy, nor even high cervical cord transection has any effect on CCK's ability to excite DA neurons. It appears that CCK's actions on the DA system are centrally mediated. In addition to examining peptide catecholamine interactions we have also used single unit recording techniques to study the effects of various benzodiazepine receptor agonists and antagonists on gamma aminobutyric acid (GABA)-sensitive neurons in the substantia nigra zona reticulata. We observed that the so-called "peripheral" benzodiazepine agonist Ro-5-4864 excited these neurons but this excitation was not reversed by the benzodiazepine antagonist RO-15-1788. In contrast, 3-carboethoxy-Beta-carboline (BCCE) excites these neurons and was reversed by Ro-15-1788. BCCE also blocks the inhibitory effect of iontophoretic GABA on these neurons while benzodiazepins, potentiate GABA.